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Cleavage, Downregulation, and Aggregation of Serum Amyloid A. | LitMetric

Cleavage, Downregulation, and Aggregation of Serum Amyloid A.

J Phys Chem B

Department of Chemistry & Biochemistry , University of Oklahoma, Norman , Oklahoma 73019 , United States.

Published: February 2020

AI Article Synopsis

Article Abstract

Various diseases cause overexpression of the serum amyloid A (SAA) protein, which in some cases, but not in all cases, leads to amyloidosis as a secondary disease. Response to the overexpression involves dissociation of the SAA hexamer and subsequent cleavage of the released monomers, most commonly yielding fragments SAA of the full-sized SAA. We report results from molecular dynamic simulations that probe the role of this cleavage for downregulating the activity and concentration of SAA. We propose a mechanism that relies on two elements. First, the probability to assemble into hexamers is lower for the fragments than it is for the full-sized protein. Second, unlike other fragments, SAA can switch between two distinct configurations. The first kind is easy to proteolyse (allowing a fast reduction of the SAA concentration) but prone to aggregation, whereas the situation is opposite for the second kind. If the time scale for amyloid formation is longer than the one for proteolysis, the aggregation-prone species dominates. However, if environmental conditions such as low pH increases the risk of amyloid formation, the ensemble shifts toward the more protected form. We speculate that SAA amyloidosis is a failure of this switching mechanism leading to accumulation of the aggregation-prone species and subsequent amyloid formation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346682PMC
http://dx.doi.org/10.1021/acs.jpcb.9b10843DOI Listing

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